The endothelium is one of the largest organs in the human body and lines the blood vessels and microcirculation of all the vital organs. As such, it functions as a massive and critical surveillance system to orchestrate recognition and host response to pathogens vial pathogen-associated molecular patterns (PAMPs) and endogenous “alarmins” via danger-associated molecular patterns (DAMPs).

Although sepsis research was conventionally focused on deleterious host-mediated inflammatory responses, it is now recognized that endothelial activation/dysfunction affecting vital organs, rather than solely inflammation per se, plays a major biological role in the pathophysiology of sepsis and associated clinical outcomes.

Despite decades of research, sepsis remains a formidable enigma and a major challenge in biomedical research. Individuals who develop sepsis and related conditions continue to experience adverse clinical outcomes and end-organ injury, including acute kidney injury (AKI), acute lung injury and the clinical syndrome of acute respiratory distress syndrome (ARDS), and multiple organ dysfunction syndrome (MODS).

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